|Title:||Prevention of Early Onset Group B Streptococcal Disease (GBS) in Neonates and Identification of Mothers who are Group B Streptococcal Carriers|
|Document ID:||Operational Circular OP 1866/04|
|Date of issue:||Thursday, 28 October 2004|
|Description:||This Operational Circular is to provide guidance for obstetricians, midwives, neonatologists, general practitioners and other relevant health care workers on the prevention of early onset neonatal group B streptococcal (GBS) disease in neonates.|
|Framework:||Public Health Policy Framework|
|Period of effect:||from 28 October 2004|
|Authorised by:||Dr Shirley Bowen, Director, Communicable Disease Control Directorate, 16-Oct-2004|
|Print version:||View print version|
|To be read in conjunction with:||
Prevention of Early Onset Group B Streptococcal Disease (GBS) in Neonates and Identification of Mothers who are Group B Streptococcal Carriers
This Operational Circular is designed to advise Department of Health staff on Departmental policies and procedures.
Group B streptococcus (GBS) has emerged as an important and frequent cause of perinatal morbidity and mortality.1-3 GBS is part of the normal bacterial flora of the gastrointestinal tract and the lower vagina. An estimated 10% - 30% of pregnant women are colonised with GBS.4 The incidence is considerably higher in indigenous populations.5 GBS colonisation of the infant is acquired during labour and delivery from the maternal genital tract in approximately 40% - 70% of culture-positive women. In the absence of antibiotic prophylaxis, approximately 1% - 2% of infants born to GBS colonised mothers will develop early onset of infection6 characterised by pneumonia and septicaemia. In this group there is a 6% fatal outcome. This risk is higher in pre-term infants.7 Additionally, group B streptococcus may cause maternal infections including urinary tract and wound infections as well as chorioamnionitis and endometritis.
RISK FACTORS FOR NEONATAL GBS
Approximately 75% of women whose babies develop GBS have one or more of the following risk factors:7
DETECTION OF CARRIAGE
An individual woman's colonisation status can fluctuate throughout pregnancy with results obtained at 35-37 weeks correlating best with culture status at birth.6 The sensitivity and specificity of the bacteriological culture test at 35-37 weeks is 87% and 96%.8 Culture specimens taken from both the rectum and lower vagina increases GBS isolation by 5% to 27% over vaginal culture alone.9-10
Two main strategies have been proposed to screen for the risk of perinatal GBS disease, a risk-based strategy and a culture-based strategy. Both strategies significantly reduced the incidence of GBS disease in the 1990s but, because no direct comparison was made between the two, evidence establishing any one strategy as more effective than the other was limited. Since this time, data from a large, non-randomised population-based study of 629,912 live births comparing the two approaches has become available.11 This study, on which the revised and updated 2002 CDC guidelines14 are based, concluded that routine culture screening for group B streptococcus during pregnancy prevents more cases of early onset disease than the risk-based approach. The study also established:
Even though the extra costs of specimen collection and processing make the culture-based strategy more expensive in the short term, overall costs between the two strategies did not differ significantly because of the savings from disease prevention.14
In recent years most hospitals in Western Australia have used a risk-based screening strategy. This appears to have been successful as the incidence of neonatal GBS infection has remained low. As already noted there is considerable debate on the most successful method of identifying women who are carriers of GBS infection. The US evidence is currently in favour of a culture-based screening approach and many institutions have already changed to this method for the prevention of GBS infection. The UK approach remains with a risk-based strategy for case identification. Recognising that the change to a culture-based method of screening presents some controversies, the imperative is that all practitioners and institutions practice have a policy in place for the detection and treatment of GBS infection in the mother and neonate. Hence, one of the two recommended strategies for the prevention of GBS disease should be followed. Given the strong evidence published in the US, Public hospitals are recommended to practice the culture-based method of screening where possible.
On the basis of the evidence, the following guidelines are recommended:
INTRAPARTUM ANTIBIOTIC PROPHYLAXIS
Intrapartum administration of antibiotics reduces the transmission of GBS and early onset GBS disease.12
The recommended intrapartum prophylaxis for GBS is IV Benzylpenicillin 1.2g initially (as a loading dose), then 600mg IV every 4 hours until delivery. Benzylpenicillin is the preferred choice because it has a narrow spectrum of activity and is therefore less likely than other antibiotics to lead to the selection of antibiotic resistant organisms.7
Penicillins, cephalosporins and related betalactam antibiotics should not be administered to individuals who have previously experienced a type I hypersensitivity reaction (i.e. any or all of anaphylaxis, bronchospasm, urticaria, angioedema) with these agents. For this group a suitable regimen is IV Clindamycin 600mg every 8 hours until delivery.
An alternative for individuals with a past history of non-type I hypersensitivity reactions to penicillin (e.g. those with a non-urticarial skin rash) is IV Cephazolin 2g as an initial dose and then 1g every 8 hours until delivery.
A careful history should always be taken regarding previous allergies and Clindamycin should be used if there is any doubt about the nature or severity of a penicillin/cephalosporin reaction.
Wherever possible antibiotics should be commenced at least four hours prior to delivery to ensure adequate prophylaxis.
As gastric emptying in labour is delayed, administration of prophylactic antibiotics by the oral route may result in incomplete, delayed or no absorption with lack of effective prophylaxis for the neonate. Further, there exists no published data of the efficacy or otherwise of intrapartum oral antibiotic prophylaxis for the prevention of GBS disease to date, whereas parenteral administration is of proven benefit. Consequently, maternal intravenous or where not practicable, intramuscular antibiotic administration is recommended. Where this is not possible, expert advice should be sought. It is recognised that some practitioners continue to use oral antibiotics in the situations previously discussed. In the absence of good evidence to the contrary, this cannot be condoned as a reasonable standard of care.
Dr Shirley Bowen
BIBLIOGRAPHY / REFERENCES:
This circular last updated: Thursday, 28 October 2004 at 12:00am